The experiments proposed here will examine the relative contributions of orosensory and postingestive effects of salt to the sodium-depletion induced, increased, need-free and need-induced salt intakes. It is postulated that the taste of salt conveys primarily positive feedback signals whereas postingestive effects of salt are primarily negative. Given this, increased salt intake could be the result of three combinations of feedback signals: 1) increased positive taste signals, no change in the negative postingestive signals, 2) no change in taste, and a decrease in the negative postingestive signals or 3) increased positive taste and decreased negative postingestive signals. The relative feedback effects of these taste and postingestive events on salt intake will be studied with the use of microstructural analysis of computer-collected, lickometer data (to study the pattern of licking), the sham-drinking gastric fistula rat and duodenal, hepatic-portal and systemic infusions of saline. These tools will allow the independent manipulation of taste and postingestive stimuli. When salt is freely available, pregnancy and lactation produce increased salt intake which persists after weaning of the litters, but not increased need-induced salt intake. Such a dissociation between increased need-free and increased need-induced salt intake has not been observed when sodium depletion is produced by Lasix and opens up the possiblity of identifying separate mechanisms for increased need-free and need-induced salt intake. The salt intakes of both sodium-depleted and multiparous females will be compared using the methods described above. The proposed experiments will also evaluate the contribution of the hormones of reproduction and of sodium conservation to the increased salt intake of the rat with a reproductive history. Thus, the specific aims for this renewal application are: 1. What are the contributions of taste and postingestive signals to the initiation, maintenance and termination of salt intake? 2. What are the mechanisms by which pregnancy and/or lactation result in increased need-free and need-induced salt intake?